Purushottam Rakhewar

Przyzębie jest morfologicznie zlożoną grupą tkanek lącznych, kt re zapewniają odżywianie i wsparcie dla struktur kostnych, cementowych i nablonkowych. Ze względu na swoje embrionalne pochodzenie, tkanki przyzębia powstają w wyniku interakcji kom rek mezenchymalnych i nablonkowych, kt re w r żny spos b reagują na r żne bodźce. Istnieje wiele potencjalnych mechanizm w regulacyjnych, kt re mogą byc zaangażowane w kontrolę funkcji kom rek w przyzębiu. Rola mediator w zapalenia jako cząsteczek sygnalizacyjnych przyzębia jest przedmiotem szczeg lnego zainteresowania, ponieważ wydają się one zdolne do regulacji wszystkich etap w homeostazy tkanek przyzębia, począwszy od regulacji zaangażowania kom rek, a skończywszy na regulacji funkcji kom rek zr żnicowanych. Poza regulacją homeostazy tkanek, mediatory te odgrywają r wnież gl wną rolę w procesach zapalnych związanych z destrukcją tkanek występujących w chorobach przyzębia, jak r wnież w regulacji adaptacyjnej odpowiedzi immunologicznej, kt ra może wplywac na progresję choroby i jej wynik kliniczny. Powszechne występowanie chor b przyzębia oraz świadomośc, że utracone tkanki mogą byc naprawione i, byc może, zregenerowane, spowodowaly znaczne zainteresowanie mediatorami inf.

Implantology is a rapidly advancing area of ​​dentistry providing a number of alternative treatment modalities for the edentulous and partially edentulous patient for more than 30 years now. Although there has been great progress in treating patients with implants as an alternative to traditional, tooth supported prostheses, maintaining healthy peri-implant tissues remains a challenge. Like natural teeth, the artificial abutments penetrate the oral mucosa and reach the contaminated oral cavity. The inflammatory lesions that develop in the tissues around implants are collectively recognized as peri-implant diseases. Inflammatory reactions associated with loss of supporting bone around an implant in function is known as 'Periimplantitis'. Accurate diagnosis and appropriate intervention are essential if implant salvage techniques are to be successful in preventing implant failure. Hence early diagnosis of peri-implantitis is very important to terminate the further progression of the diseases and for establishment of good osseointegration. Current book is highlighting all the possible treatment modalities about hard tissue management in periimplantitis.

Peri-implantitis lesion can be diagnosed early on the radiograph by detecting bone loss around the implant. Implant mobility indicates the final stage of peri-implant disease. It is evident that peri-implant disease should be recognized earlier, to allow intervention before a substantial portion of the supporting bone is lost. Therefore, diagnostic procedures used around implants, should include sensitive parameters to detect early signs and symptoms of inflammation.the microbiota associated with failing dental implants is similar to the flora commonly associated with periodontally involved teeth, and the main cause of periimplantitis is dental plaque. Acceptable techniques for the diagnosis of peri-implantitis and its associated bone loss remain clinical probing and parallel technique radiographs. Clinical probing is accurate only if the prosthetic superstructure is removed, whereas retention of the superstructure may aid in placement of radiographic positioning devices. Clinical mobility is a late diagnostic finding of low sensitivity. For satisfactory long term results, the underlying etiology, as in all therapy, must be identified and corrected.

The periodontium is a morphologically complex group of connective tissues that provide nutrition and support for bony, cemental, and epithelial structures. Based on its embryonic origin, the periodontal tissues form by the interaction of mesenchymal and epithelium cells that respond differently to a variety of stimuli. A large number of potential regulatory mechanisms exist which may be involved in the control of cell function in the periodontium. The role of inflammatory mediators as signaling molecules of periodontium is of considerable interest as they appear to be able to regulate all stages of periodontal tissue homeostasis from specifying cell commitment to regulating differentiated cell function. Apart from regulating tissue homeostasis, these mediators also play a central role in the inflammatory processes associated with tissue destruction occurring in periodontal disease as well as regulation of the adaptive immune responses that might govern disease progression and clinical outcome. The widespread occurrence of periodontal diseases and the realization that lost tissues can be repaired and, perhaps, regenerated has generated considerable interest in the inf mediators.

The role of regenerative periodontal therapy is the reconstitution of lost periodontal structures, ie, the new formation of root cementum, periodontal ligament, and alveolar bone. This text is about the enamel matrix proteins (derivatives) which represent a step towards more predictable regeneration. It introduces the scientific and biological background of the enamel matrix proteins its formulation, composition, mode of action, the role of the enamel matrix derivative in periodontal regeneration and its clinical application in various scenarios.

Periodontal pockets are favorable area within the gums created by periodontopathic pathogens where access to routine cleaning are difficult leading to destruction of soft tissues supporting teeth and clinical attachment. Even though mechanical debridement removes plaque which contains microorganisms, it's impossible to completely eradicate all virulence factors; therefore, antibacterial therapy is recommended as supplementary measure. In conjunction with scaling and root planing, the adjunctive use of local drug delivery may enhance the results in sites that don't respond to conventional therapy. Local drug delivery systems with controlled release properties have the potential to be used as a therapeutic component in the management of periodontal diseases